Headlines today are pretty scary for the estimated one third of 16-49 year old women in the UK who use hormonal contraception, warning that doing so could ‘double the risk of brain tumour’. But these tumours are so rare that a doubling in risk actually only equates to one extra case per 50,000 women taking the contraception per year.

Hormonal contraceptives are very widely used in the UK, and provide a near-perfect method of birth control. A story that suggests they are harmful could lead women away from using them, potentially stopping any form of birth control at all, and increasing their risk of unwanted pregnancies and the health risks that can go along with that.

The researchers who conducted this study used a case-control design. They had access to data from the entire population of Denmark, and used the National Cancer registry to find instances of glioma brain tumour in women aged 15 to 49, between 2000 and 2009. In this sample, they found 317 cases of brain tumour. This roughly equates to 5 women per 100,000, per year (by comparison, breast cancer affects 125 UK women per 100,000).

Some of these people will use hormonal contraception, and some won’t. In fact, of the 317 people with glioma, and the 2126 controls used as a comparison group, just over half used hormonal contraception.

Controls are the group of people without brain tumours who are needed to compare to those who did get tumours, to see whether contraceptive use differs between the groups. How these are selected is hugely important, as it’s easy to introduce bias in to the design if this group are different to the group of cases. These controls were randomly sampled from the Danish female population, and were matched on age, to the nearest year, with 8 controls being matched to every case.

Using these data, the authors of the study found that women who developed gliomas were more likely to have used hormonal contraception than those who did not, after taking in to account years of schooling, and history of allergy or asthma.

Does this mean hormonal contraception caused the increased risk? It’s not possible to tell from these findings, as the authors of the study make plain in their paper. Whenever you observe groups of people, rather than randomly split them to either receive the intervention or not, you can never be completely sure that there aren’t other differences between the groups that could be causing the association seen. For example, obesity is thought to impact on glioma rates, but data on this was not available for the women included in this study.

Aside from the findings in this paper, there is also some evidence that hormonal contraception could be protective against ovarian cancer, cancer of the womb, and bowel cancer, all of which are more common than these brain tumours.

So while this paper suggests that hormonal contraception use might increase the risk of these specific and rare tumours, it’s certainly not definitive proof, and even if it was, women shouldn’t make decisions about their contraception based solely on this paper.

Lori Simons took the bright orange pill at 3 a.m. Eight hours later, doctors sliced into her brain, looking for signs that the drug was working.

She is taking part in one of the most unusual cancer experiments in the nation. With special permission from the Food and Drug Administration and multiple drug companies, an Arizona hospital is testing medicines very early in development and never tried on brain tumors before.

Within a day of getting a single dose of one of these drugs, patients have their tumors removed and checked to see if the medicine had any effect. If it did, they can stay on an experimental drug that otherwise would not be available to them. If it did not, they can try something else, months sooner than they normally would find out that a drug had failed to help.

"They don't lose any time," said Dr. Nader Sanai, the doctor leading the study at Phoenix's Barrow Neurological Institute.

Time is everything for people with glioblastoma, the most common and deadly type of brain tumor, the kind that killed Massachusetts Sen. Edward M. Kennedy in 2009. Even when surgeons think they got it all, the cancer usually grows back and proves fatal. The few drugs to treat these tumors have little effect — median survival is about 14 months.

"We've had an endless string of failures" to find better ones, Sanai said.

His study is for people whose cancer came back. Doctors use a stored sample from the original tumor to see if its growth is driven by any genes or pathways targeted by one of the experimental drugs in development. If so, they give that single dose of the new drug before surgery to remove the new tumor.

Then, the tumor tissue is examined under a microscope to see if the drug had its intended effect on the genes or pathways.

So far, the study has tested one drug from AstraZeneca PLC in four patients. Another drug, from Novartis, will be added soon.

"We're trying to develop a portfolio of these" so there are many possible drugs available for new patients under a single "umbrella" study, Sanai said.

It is called a "phase zero" clinical trial because it comes before the usual three-phase experiments to determine a drug's safety, ideal dose and effectiveness.

"We view this as a great thing, as something that will produce better drugs that have greater chance of working," said Dr. Richard Pazdur, cancer drug chief at the FDA.

"Cost potentially will go down and certainly time will go down" for companies testing new drugs this way and patients seeking something that will help, he said.

Dr. James Doroshow was involved in the only previous studies like this, done at the National Cancer Institute.

In the past, "if you had a new drug, you'd give it to a patient, you'd measure the blood levels, but very rarely would you have a way to know whether the presumed method of action was working in the patient," he said.

The Arizona study gives a way to check that, because the tumor is removed right after the first dose is given. And if the drug does not work in any or few of the people who get it, the study could spare others a futile treatment, and limit the time and money a drug company invests.

"If you're going to fail, you want to fail early and fail fast before you put thousands of patients into randomized trials," Doroshow said.

A novel radioguided surgery technique could quickly and effectively identify residual cancer cells during brain tumor surgery, with low radiation exposure for both patients and surgeons. The study, featured in the January 2015 issue of the Journal of Nuclear Medicine, reports that Y-90 DOTATOC, a beta-minus-emitting tracer, can effectively delineate the margins of meningiomas and high-grade gliomas.

Radioguided surgery (RGS) allows the surgeon to evaluate the completeness of a tumor resection while minimizing the amount of healthy tissue removed. During the procedure, a surgeon is provided with vital and real-time information on the location and extent of the lesion that allows better assessment of the resection margins. The technique uses a radiolabeled tracer preferentially taken up by the tumor to discriminate cancerous tissue from healthy organs, as well as a probe sensitive to the emission released by the tracer, to identify in real time the targeted tumor focus. The radiopharmaceutical is administered to the patient before surgery.

"This research relates to a completely innovative radioguided surgery technique: the use of a beta-minus-emitting tracer," states lead researcher Riccardo Faccini. "This is a change in paradigm because RGS currently uses only gamma and beta-plus-emitting isotopes. The new technique uses Y-90-labeled DOTATOC--a tracer that traditionally is used for molecular radiotherapy--for diagnostic purposes."

In the study, uptake and background from healthy tissues were estimated on Ga-68 DOTATOC positron emission tomography (PET) scans of 11 meningioma patients and 12 high grade glioma (HGG) patients. A dedicated statistical analysis of the images was completed and validated. The feasibility study was performed using full simulation of emission and detection of the radiation, accounting for the measured uptake and background rate. All meningioma patients but one, who had an atypical extracranial tumor, showed high uptake of DOTATOC. Uptake of Y-90 DOTATOC in meningiomas was high in all studied patients. Uptake in HGGs was lower than in meningiomas but was still acceptable for RGS. Funding for the study was provided by Italian institutions Universita' di Roma La Sapienza, Istituto Nazionale di Fisica Nucleare, Istituto Italiano di Tecnologia, Centro Fermi Museo Storico della Fisica, and Istituto Europeo di Oncologia.

"We are setting up clinical tests of RGS with beta-minus radiation on meningiomas, based on their known high receptivity for DOTATOC," Faccini said. "This study suggests that the next step will be to try the technique on gliomas, which will be more challenging, but feasible and definitely clinically interesting. In parallel with this technique, we are also developing a surgical probe customized for the problem, which could in the future extend the applicability of the method to endoscopy or laparoscopy."

Meningiomas are tumors that grow on the delicate outer covering of the brain. According to the Brain Science Foundation, meningiomas account for approximately 33.8% of all primary brain tumors, making them the most common type. Gliomas, which are malignant tumors that commonly invade adjacent tissue and spread through the central nervous system, represent about 17.1% of all primary brain tumors and about 70.5% of all astrocytomas.

Pancreatic cancer is one of the deadliest forms of the disease. The American Cancer Society's most recent estimates for 2014 show that over 46,000 people will be diagnosed with pancreatic cancer and more than 39,000 will die from it. Now, research led by Timothy J. Yen, PhD, Professor at Fox Chase Cancer Center, reveals that one reason this deadly form of cancer can be so challenging to treat is because its cells have found a way to sidestep chemotherapy. They hijack the vitamin D receptor, normally associated with bone health, and re-purposed it to repair the damage caused by chemotherapy. The findings, which will be published in the January 3 issue of the journal Cell Cycle, raise hopes that doctors will one day find a way to turn this process against the tumor and help chemotherapy do its job.

Most patients diagnosed with pancreatic cancer receive a drug called gemcitabine, which works by preventing cells from replicating their DNA -- thus stopping tumor cells from dividing and causing them to die off. Sadly, many patients die within a few months, often because their cancer finds a way to work around treatment. But how does that happen? "Maybe there is something we don't understand about how gemcitabine works," says Dr. Yen. "More likely, cancer cells have found a way to avoid DNA-damaging drugs."

To determine how pancreatic cancers sidestep chemotherapy and the effects of gemcitabine, Dr. Yen and his colleagues removed every one of the ~24,000 genes, one by one, in pancreatic cancer cells, exposed the cells to gemcitabine, and noted which gene "knockout" caused cells to be more sensitive to the drug.

One of those "knocked-out" genes was particularly important, namely, the gene for a protein which normally binds to vitamin D. "When we inactivated this vitamin D receptor in cancer cells and added gemcitabine, almost all of them died," says Dr. Yen.

That's when the researchers realized they had identified a key mechanism driving chemotherapeutic effectiveness against pancreatic cancer. "If we find a drug that inactivates the vitamin D receptor, it may allow gemcitabine to selectively kill pancreatic cancer cells while leaving healthy cells unharmed," says Dr. Yen. "Patients would just need to drink lots of milk or take calcium supplements to make sure their bones stay healthy."

Although the precise role of the vitamin D receptor in pancreatic cancer remains uncertain, it's clear that pancreatic cancer cells need it, says Dr. Yen. "Cancer cells are good at finding ways to survive," he explains. "We suspect that cancer cells hijacked the vitamin D receptor and reassigned it to perform other cellular functions, such as by repairing DNA damage caused by gemcitabine so the cancer can continue to divide and spread."

Although pancreatic cancer cells need the vitamin D receptor to survive, other normal cells don't, which Yen says is good news for patients because future cancer treatments can knock out the receptor without causing too much collateral damage or side effects, as long as patients take calcium supplements to keep their bones healthy.

"By knocking out the vitamin D receptor, we could inactivate that DNA repair process that is allowing drug-treated tumor cells to live. As a result, we could eliminate more cancer cells at the outset," says Dr. Yen. "The Pancreatic Cancer Action Network has launched an initiative to double patients' survival by 2020; with this new finding, we believe it's a step in the right direction."

Who is online

Users browsing this forum: No registered users and 1 guest

You cannot post new topics in this forumYou cannot reply to topics in this forumYou cannot edit your posts in this forumYou cannot delete your posts in this forumYou cannot post attachments in this forum